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IgE 受体桥接诱导的触发信号的生化分析

Biochemical analysis of triggering signals induced by bridging of IgE receptors.

作者信息

Ishizaka T

出版信息

Fed Proc. 1982 Jan;41(1):17-21.

PMID:6276231
Abstract

Bridging of IgE receptors on rat mast cell plasma membranes induces phospholipid methylation and a monophasic increase in cyclic AMP. The stimulation of phospholipid methylation in the plasma membrane appears to be intrinsic to the processes leading to Ca2+ influx and histamine release. Evidence was obtained that IgE receptors are closely associated with methyltransferases and adenylate cyclase in the plasma membranes. The activation of one enzyme is regulated by the other. An increase in the cyclic AMP level before receptor bridging suppressed phospholipid methylation. On the other hand, inhibition of phospholipid methylation may affect the initial rise in cyclic AMP. Our experiments also indicated that bridging the receptor activates a membrane-associated proteolytic enzyme. Inasmuch as the inhibition of the enzyme activation results in the suppression of both phospholipid methylation and initial rise in cyclic AMP induced by receptor bridging, the proteolytic enzyme may be involved in the activation of methyltransferases and adenylate cyclase.

摘要

大鼠肥大细胞质膜上IgE受体的桥联可诱导磷脂甲基化以及环磷酸腺苷(cAMP)的单相增加。质膜中磷脂甲基化的刺激似乎是导致Ca2+内流和组胺释放过程所固有的。有证据表明,IgE受体与质膜中的甲基转移酶和腺苷酸环化酶密切相关。一种酶的激活受另一种酶的调节。受体桥联前cAMP水平的升高抑制了磷脂甲基化。另一方面,磷脂甲基化的抑制可能会影响cAMP的初始升高。我们的实验还表明,受体桥联可激活一种膜相关蛋白水解酶。由于该酶激活的抑制导致受体桥联诱导的磷脂甲基化和cAMP初始升高均受到抑制,因此该蛋白水解酶可能参与甲基转移酶和腺苷酸环化酶的激活。

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